Acute Chest Pain

Prof. Maria Dorobanu, MD,

FESC, FACC
Medical Emergencies VIth year
Causes of acute chest pain
System Syndrome

Cardiac Acute coronary syndrome

Pericarditis
Vascular Aortic dissection
Pulmonary embolism
Pulmonary hypertension
Respiratory Pleuritis/pneumonia
Pneumothorax
Gastrointestinal Esophagitis
Peptic ulcer
Pancreatitis
Chest wall Costochondritis
Cervical radiculopathy
Thoracic trauma
Infectious Herpes zoster

Psychological Panic attack Braunwad, 2007, p1196

Causes of acute chest pain

Acute coronary syndrome with/without ST elevation

Acute aortic dissection
Pulmonary embolism
Pneumothorax
Acute pericarditis
Pneumonia/pleuresy
Thoracic radiculopathy
Tietzes syndrome
 Acute coronary syndromes
(ACS)

non- ST elevation With ST elevation

NSTEMI

Unstable angina Myocardial infarction

non-Q Q-AMI
AMI
Causes of acute chest pain

Acute coronary syndrome with/without ST elevation

Acute aortic dissection
Pulmonary embolism
Pneumothorax
Acute pericarditis
Pneumonia/pleuresy
Thoracic radiculopathy
Tietzes syndrome
 Signs and symptoms
Acute coronary Aortic PE Pneumotho Pneumonia/ Radiculopat Acute
syndromes dissection rax pleuresy hy pericarditis

Character of +++ +++ + +++ + ++ ++

the pain
continuous
Vegetative ++ +++ ++ + + + +
symptoms

Dyspnea +++ +++ _

(Pulmonary
edema)
Hemoptysis ++ _ _ _ _
(Pulmonary
edema)
Cyanosis _ ++ _ _ _
(Pulmonary
edema)
 Clinical examination
ACS Aortic PE Pn.thorax Pneumonia/ Radiculitis Acute
dissection pleuresy pericarditis

BP () N

Pulse N

Left ventricular
dysfunction EPA unilat _ _ _ _

Right ventricular _
dysfunction ++ _ _

Condensation
syndrome
_ _ _ +++ _ _

Hyperresonance _ _ _ ++ _ _
 ECG in acute thoracic pain

Acute coronary Aortic PE Pneumotho Pneumonia/ Radiculopat Acute

syndromes dissection rax pleuresy hy pericarditis

ECG +++ ++ _ _ ++
Localization of MI on ECG
 ECG CHANGES IN
PULMONARY EMBOLISM
Sinus tachycardia
minor or major RBBB
Right axis deviation
T wave inversion in DIII, AVF,V1-V4
ST, QIII, T3
AF or AFl
NON STEMI ST ELEVATIONS
NON STEMI ST ELEVATIONS
 False positive ECG for MI
1. LBBB
2. LVH
3. Pericarditis
4. Myocarditis
5. PTE
6. Hyperkalaemia
7. Post - cardioversion
8. Brugada syndrome
9. Cerebral haemorrhage
10. Early repolarization
11. Normal varian
 Biological samples for
chest pain
MI Aortic PTE Pneumotho Pneumonia/ Neuralgia Acute
dissection rax pleurisy pericarditis

Cardiac
troponin
+++ _ _ _ _ _ _

Specific
enzymes
CK-MB
+++ _ _ _ _ _

Inflammatory
syndrome
/+ _ + _ +++ _ ++
Other causes of troponin I or T elevation

Myopericarditis
Severe trauma
Congestive heart failure
Pulmonary thromboembolism
Sepsis
Kidney failure
Collagen diseases
 Radiologic examination for
chest pain
acute coronary Aortic PTE Pneumotho Pneumonia/ Neuralgia Acute
syndrome dissection rax pleurisy pericarditis

X-ray _ () + ++ +++ +++ _

 Special investigations for
chest pain
UA MI Aortic PTE Pn.thorax Pneumonia/ Neuralgia Acute
dissection pleurisy pericarditis

Cardiac
ultrasound + ++ + _ _ _ ++

CT _ _ ++ ++ _ /+ _

Scintigraphy _ ++ _ ++ _ _ _ _

Angiography ++ ++ ++ ++ _ _ _ _

MRI _ _ + + _ _ _ _
CT IN PULMONARY EMBOLISM
 PTE:
Myocardial perfusion and ventilation
scintigraphy
Coronary angiography of MI
Acute aortic dissection
Acute aortic dissection
Acute aortic dissection
Coronary angiography in UA
Aortography :
 Conclusion:
Differential diagnosis of chest
pain is sometimes almost
impossible
CHEST PAIN
-second part-
TREATMENT
UNSTABLE ANGINA
TREATMENT IN
CORONARY INTENSIVE
CARE UNIT
 Treatment goals
pain relief
prevention of AMI
preservation of viable myocardium
preventing death

identifying and treating the trigger

determining prognosis
identification and treatment of coronary risk factors
preventing relapses
 Immediate general
measures
Admission to coronary intensive
care unit
O2 administration
venous line
monitoring
calming the patient
bed rest
quiet environment
Pain relief
Nitroglycerin
Algocalmin(1 f. diluted
iv.)
Piafen (1 f. in perfusion)

Morphine (2-4 mg
diluted with antiemetic and
repeated at 15 min)
Mialgin analgesic solution:
1f. 100mg diluted to 10 ml,
1ml/min repeated at 10 min
until it relieves the pain)
 Antiplatelet medication
1. Aspirin
325g/day initial (act. in 15) continued with 75-150mg/day

. P2Y12 INHIBITORS
2. Clopidogrel (Plavix)(ADPdep)
Loading dose of 300 mg on the first day followed with 75mg/day
Comparable results to aspirin

3. Prasugrel only to patients that will receive invasive

angiographic evaluation
50 mg loading dose on the first day followed by 10 mg / day
 Antiplatelet medication

4. Ticagrelor administrable no matter the therapeutic

attitude
Loading dose of 180 mg on the first day followed by 2 x 90 mg /
day

5 . Abciximab, tirofiban, eptifibatide

mechanism: inhibits GPIIbIIIa-fibrin binding, when administered
in perfusion
action: inhibits strongly and specifically platelet aggregation in the
acute phase
 Anticoagulant treatment
1. Heparin
action:
Antithrombotic, stabilizes the endothelium

Advantages:
prevents formation of new thrombi
decreases the incidence of angina, silent ischemia, AMI and death
potentiates the effect of aspirin
Disadvantages:
does not act on pre-existing thrombi
rebound at discontinuation
bioavailability varied and increased variability of response
 Anticoagulant treatment
1. Heparin
Dose
initial IV bolus of 60 IU / kg (maximum 4000 IU)
followed by continuous infusion of 12 IU / kg / hour (maximum
1000 IU)
under control every 4-6 hours and dose adjustments to achieve
an aPTT between 50 and 70 s (1.5 - 2 x N)

AR:
Haemorrhages
thrombocytopenia
tissue necrosis
osteoporosis
Antidote
protamine sulfate
Calciparin- can be administered sc 1mg/kgc/12h
 Anticoagulant treatment
2. Low molecular weight heparin
Enoxaparina (Clexane)
Fondaparinux (Arixtra)

Mechanism:
inhibits Xa factor

Advantages:

according to studies is more effective than standard heparin

does not require biological monitoring of anticoagulation
good bioavailability at sc administration

Dose:
Clexane: 1 mg/kgc at 12h
 Anticoagulant treatment
3. Direct thrombin inhibitors
Bivalirudin alternative for heparin at patients with high bleeding
risk
Mechanism:
Inhibits directly thrombin activation
Advantages:
Similar efficacy with lower bleeding risk when compared with
unfractionated heparin and low molecular weight heparin in
patients with ACS moderate and high risk class benefiting from
early invasive treatment (PCI)

Disadvantages:
Exclusively reserved for patients with ACS moderate and high
risk class benefit of early invasive treatment (PCI)
 Antiischemic treatment
1. Beta-blockers
Advantages:
diminishes ischemic phenomena
decreases of crisis frequency
prevents MI and death
Mec
decreasec VA, BP, O2 consumption, contractility
increasea the subendocardium flow
Dose:
PO: bisoprolol 5-10 mg/metoprolol 50-200 mg / day adjusted for VA
of 50-60 bpm and is a long-term treatment
IV: esmolol 50-250 ug / kg / min only at patients with high risk,
significant ST changes, tachycardia
 Antiischemic treatment
2. Nitroglycerin
Mec-Adv:
Coronaro-dilatation => reduces ischemic phenomena, relieves angina
Veno-dilatation => decreases pre-load, ventricular volume, PCAP, with
improvement HF phenomena
systemic arterio-dilatation (in a smaller degree) => decreasing post-load
Disadvantages:
not conclusive evidence in favor of lowering the risk of MI or death
Administration:
Sublingual -3 tb initially, followed by iv perfusion at patients with persistent
pain, hypertension or HF phenomena
Iv perfusion :
Initial: 5-10 mg / min
increases at 10 min with 5-20 g / min, depending on symptoms and the value of BP
Maximum dose: 400 g/min
Develops tolerance tachyphylaxis phenomenon => lasts up to 48 hours
continue with PO treatment or NTG patch (change at 12 h but leave 4-6h breaks
between them)
 Antiischemic treatment
3. Ca-blockers

Advantages
Coronaro-dilatation

chrontropic, dromotropic and inotropic negative effects

peripheral vasodilation

A. Non-dihydropyridines (diltiazem,verapamil)
Slows SAN activity

do not associate with beta blockers (additive negative dromtrop / inotrop

effect => BAV risk, risk of worsening LV systolic dysfunction and HF)
can be used when patients can not tolerate beta blockers
B. Dihydropyridines (nifedipine, amlodipine, nicadipine)
may be associated with beta-blockers

short-acting Nifedipine is contraindicated (increases ischemia by coronary steal

phenomenon => increases mortality)
 Clinical suspicion of ACS
Clinical ex., ECG, echo, monitoring, biology

Without persistent
persistent ST
ST ASA, Heparin, -bl, nitrates

Thrombolysis High risk Low risk

PCI
2-nd Tn dosing

GP IIb/IIIa inh. negative

positive
Coronarography twice

Stress test
Coronarography
Prompt diagnosis
Symptoms 112 ambulance arrival
T1 + T2 +
T3

primary PCI diagnosis recognition

or Establishment of the
establishment of thrombolysis first therapeutic measures
Optimum: T< 3h Transport to hospital
+
T4
T =

Hospitalization tests
 Reperfusion therapy:

Primary PCI
PCI (percutaneous coronary intervention) - Recommended as
first-line therapy for revascularization, where available
Advantages:
Restores normal epicardial coronary flow in> 90% of cases
Increased survival compared to thrombolysis
Lower rate of intracranial bleeding and recurrence of MI
compared to thrombolysis
Can be performed in patients with contraindications to
thrombolysis
Disadvantages:
increased costs
low accessibility
IMA LEFT MAIN
DIAGNOSTIC
IMA LEFT MAIN
POST PCI
Thrombolytic treatment

NOT in unstable angina !

CI because of the increased risk
of AR (bleeding) without obvious
benefit in decreasing mortality
(TIMI IIIB trial)
 3. Reperfusion therapy:
Indications

ST elevation> 1 mm in at least two adjacent

bipolar derivations or 2 mm in at least two
adjacent precordial leads
OR
new installed LBBB with symptoms suggestive
for AMI

Clinical onset is not more than 24 hours ago

Without C1
 Thrombolysis:
Absolute contraindications
History of haemorrhagic stroke no matter
when; other tipes of stroke or
cerebrovascular events in the past year
Known intracranial neoplasm
Active internal bleeding (does not include
menses)
Suspicion of aortic dissection
 Fibrinolytics
Contraindications:
Active internal bleeding (<21days)
CNS injury in last 3 months (stroke, neoplasm,
aneurysm, recent trauatism, surgery)
General surgery / major injury in <14days
aortic dissection
Severe uncontrolled hypertension
haemorrhagic diathesis
prolonged resuscitation
lumbar puncture in <7days
arterial puncture at non-compressible sites
 Thrombolysis: Relative
contraindications. Precautions.
Severe uncontrolled hypertension at the time of presentation (BP>
180/110 mmHg)
History of stroke or intracranial pathology, not included in absolute
contraindications
Therapeutic-dose anticoagulation (INR> 2.3); known
haemorrhagic diathesis
Recent trauma (in the last 2-4 weeks) including head trauma,
prolonged cardiopulmonary resuscitation (> 10 min), major
surgery in the last 3 weeks
Non-compressible vascular punctures
Recent internal bleeding (2-4 weeks)
Exposure to Streptokinase from 5 days to 2 years ago or with a
history of allergic reaction
pregnancy
Active peptic ulcer
Historic of severe chronic hypertension
 Fibrinolytics
NB!: Dedicated intravenous line
r-tPA:

-2 types of administration: rapidly (15mg bolus, then 50 mg in

30 min., then 35 mg in 1h), or usual (60 mg the first hour,
then 20 mg / h for 2 hours)
- followed by heparin at least 48h
SK:

-1.5 x 106 U PIV in 1h (* 30 min)

-100 mg HSHC administered before
-immunogenic
Reteplase: 10 U bolus in 2 min, then another 10 U after 30
min
Tenecteplase: 30-50mg bolus
ADJUNCTIVE THERAPIES

ACE inhibitors

Statines

Glicemic control
 Complications of MI
majore:
rhythm and conduction disorders
pump dysfunction
persistent periinfarct myocardial ischemia
thromboembolism
Mechanical complications:
cardiac rupture (IVS ,free wall, pillar)
ventricular aneurysm

minore:
periinfarct pericarditis (serofibrinous)
Risk evaluation in the acute
phase of AMI
Killip functional classification
Functional class Clinical signs Acute mortality

I
No LVF 5-7%
(uncomplicated AMI)
dyspnoea
II
pulmonary stasis 10-15%
(HF mild / moderate)
protodiastolic gallop
III
APE 20-50%
(severe CHF)
IV hBP, peripheral
hypoperfusion and of 60-80%
(cardiogenic shock) vital organs
Risk evaluation in the acute
phase of AMI
Forrester classification
I B: Hyperdinamic

II : pulmonary
I A: compensated
congestion
2,2

III: isolated IV: cardiogenic

systemic shock
hypoperfusion
18

Pulmonary capillary pressure (mmHg)

Aortic dissection

Surgical treatment
first choice in acute proximal
dissection or complicated by organ
failure, rupture or impending rupture
acute dissection
c-ind.: 1 month old or type III without
compromised organ
 Aortic dissection
Medical treatment
objectives:
stop progression of hematoma
pain relief
Physiopathology:
lower BP (120-130 mm Hg)
decrease LV contractility
associated with with negative inotropic vasodilator
nitroprusside 1-10 g/min + Propranolol (0,5 mg iv slowly, then 1
mg/5 min so that VA=60-80/min
trimetaphan
labetalol
enalapril (in cases with refractory hypertension) 1-2 mg/4-6h
Calcium blockers: Nicardipine
 PTE treatment
Thrombolytics
in massive PTE
SK (250.000 U n 30 min. then 100.000 U/h) or UK
(4400U/kg in 10 min then 4400/kg/h) or tPA
Heparin
moderate / small PTE
bolus 10.000 U, then piv 1500-2000 U/h
Oral anticoagulants
Adjuvant measures:
oxygen
assisted ventilation
dobutamine (in case of cardiogenic shock)
NSAIDs (if pleuretic pain persists)
PTE treatment

Surgery treatment
pulmonary embolectomy
Note: imminent cardiogenic shock
high mortality
Prophylaxis
Secondary: inferior vena cava interruption (clip
ADAMS / filters)
Primary: tackling the risk factors for PTE
Treatment of acute pericarditis

Etiologic :
NSAIDs
antibiotic
stopping anticoagulants
anticancer therapy
tuberculostatics
corticosteroids (1 mg / kg / day with progressive
dose reduction)
Pathogenic :
in forms with CT : pericardiocentesis
Pneumothorax treatment
Lung decompression:
required in tension pneumothorax
Air decompression
aspiration
emergency pleural puncture
Oxygen therapy:
in forms with respiratory failure
Reexpansion of the lung:
usually spontaneously if pleural fistula is closed
oxygen in large quantities speeds reabsorption
drainage
Symptomatic medication
Treatment of pneumonia /
pleurisies
etiological
pathogenic

Neuralgia treatment
antiinflammatory
analgesics
THANK YOU FOR YOUR
ATTENTION!